Plants are exposed to numerous denizens of their environment, including bacteria, viruses, fungi, and nematodes. Although many of the interactions between these organisms and plants, particularly via the roots of the plants, are beneficial, many of the interactions are harmful to the plants. The decimation of agricultural crops, ornamental plants, and other plants by diseases caused by plant pathogens is a worldwide problem that has enormous economic impact.
Damage to plants is caused by pathogens of multiple genera. These genera include Alternaria, Ascochyta, Aspergillus, Botrytis, Cercospora, Colletotrichum, Diplodia, Erwinia, Erysiphe, Fusarium, Gaeumanomyces, Helminthosporium, Macrophomina, Magnaporthe, Mycosphaerella, Nectria, Peronospora, Phoma, Phymatotrichum, Phytophthora, Plasmopara, Podosphaera, Pseudomonas, Puccinia, Puthium, Pyrenophora, Pyricularia, Pythium, Rhizoctonia, Scerotium, Sclerotinia, Septoria, Thielaviopsis, Uncinula, Venturia, Verticillium, and Xanthomonas. 
Macrophomina, Magnaporthe, Mycosphaerella, Nectria, Peronospora, Phoma, Phymatotrichum, Phytophthora, Plasmopara, Podosphaera, Pseudomonas, Puccinia, Puthium, Pyrenophora, Pyricularia, Pythium, Rhizoctonia, Scerotium, Sclerotinia, Septoria, Thielaviopsis, Uncinula, Venturia, Verticillium, and Xanthomonas. 
Many chemical compounds have been developed to combat these various pathogens. The activity of these compounds is typically limited to several species. As a consequence of the large number and diversity of plant pathogens, these compounds have not provided an effective solution to limiting infections in plants.
An alternative approach to controlling pathogenic infections in plants involves exploiting the natural defense mechanisms of plants to confer resistance. Many plants have developed natural resistance to some pathogens. However, resistance may be limited to certain genera of pathogens, or crops of agronomic interest may not exhibit sufficient resistance. Thus, natural plant defenses often do not provide sufficient protection against pathogens. By broadening the spectrum of pathogen defense or strengthening the defense response, it may be possible to enhance existing resistance mechanisms and promote pathogen defense in otherwise susceptible plants.
When present and active, the natural defense mechanisms of plants can be highly effective in preventing pathogen colonization and disease. Resistance is multi-tiered, with passive and active, constitutive and inducible elements.
Following the invasion of a plant by a potential pathogen, the pathogen either successfully proliferates in the host, causing associated disease symptoms, or its growth is halted by the defenses of the host plant. One such defense is the hypersensitive response (HR), rapid apoptotic cell death near the site of the infection that correlates with the generation of activated oxygen species, production of antimicrobial compounds, and reinforcement of host cell walls (Dixon and Lamb, Annu. Rev. Plant Physiol. Plant Mol. Biol. 41:339-367, 1990). Other defenses include systemic acquired resistance, which effectively protects the plant against subsequent attack by a broad range of pathogens (Ryals et al., Proc. Natl. Acad. Sci. USA 92:4202-4205, 1995).
Pathogens that elicit an HR on a given host are “avirulent” on that host, the host is “resistant,” and the plant-pathogen interaction is “incompatible.” If a pathogen proliferates and causes disease to the host, the pathogen is “virulent,” the host is “susceptible,” and the plant-pathogen interaction is “compatible.”
In many cases in which strains (“races”) of a particular fungal or bacterial pathogen differ regarding virulence on various cultivars (or wild accessions) of a particular host species, avirulent strains of the pathogen, but not virulent strains, possess one or more avirulence (avr) genes corresponding to “resistance” genes in the host. Resistance gene products are activated in response to pathogen signal molecules termed elicitors, production of which is controlled by pathogen avirulence genes. This observation is the basis for the “gene-for-gene” model of plant disease resistance (Crute et al., pp. 197-309 in Mechanisms of Resistance to Plant Disease, Fraser, ed., 1985; Ellingboe, Annu. Rev. Phytopathol. 19:125-143, 1981; Flor, Annu. Rev. Phytopathol. 9:275-296, 1971; and Keen et al., in Application of Biotechnology to Plant Pathogen Control, Chet, ed., John Wiley & Sons, 1993, pp. 65-88).
Normally avirulence and resistance genes are organized in functional pairs. A given resistance gene is generally effective only against pathogen strains that express a specific cognate avirulence gene (Flor, Annu. Rev. Phytopathol. 9:275-296, 1971; Keen, Annu. Rev. Genet. 24:447-463, 1990). However, exceptions to this rule exist. For example the Arabidopsis RPM1 gene product (Grant et al., Science 269:843-846, 1995) is involved in the recognition of elicitors produced by P. syringae expressing the avirulence genes avrRpm1 or avrB (Bisgrove et al., Plant Cell 6:927-933, 1994), suggesting that resistance gene products may function as common points in transduction of distinct pathogen signals.
A number of avirulence genes have been cloned. Many cloned avirulence genes have been shown to correspond to individual resistance genes in the cognate host plants and confer an avirulent phenotype when transferred to an otherwise virulent strain. A number of plant disease resistance genes have also been cloned. Similar features have been discovered among many of these resistance genes, in spite of the diversity of pathogens against which they act. These features include a leucine-rich-repeat (LRR), a motif found in a multitude of eukaryotic proteins with roles in signal transduction (Kobe and Deisenhofer, Trends Biochem. Sci. 19:415-421, 1994). The LRR motif is thought to be involved in protein-protein interactions and may allow interaction with other proteins that are involved in plant disease resistance. In addition, sequences predicted to encode nucleotide binding sites and leucine zippers are shared among many resistance genes (Dangl, Cell 80:383-386, 1995; Staskawicz et al., Science 268:661-667, 1995). These motifs are present and similarly organized among resistance gene products from plants as diverse as tobacco, tomato, rice, flax, and Arabidopsis, suggesting a common mechanism underlying disease resistance signal transduction throughout the plant kingdom.
The local perception of pathogen attack is conveyed to distant tissues via a transmissible signal that involves salicylic acid (SA), further activating gene expression and conditioning a state known as systemic acquired resistance (SAR). It has subsequently been found that resistance can be expressed near the region of pathogen attack, as local acquired resistance, or can be induced systemically, depending on triggering signal and plant species. Thus, the systemic and local responses collectively are referred to as acquired resistance (AR). Establishment of AR is a powerful line of plant defense because it can provide broad-spectrum resistance against viral, bacterial, and fungal challenges that would otherwise cause disease. The AR response triggers the transcriptional activation of a suite of genes encoding pathogenesis-related (PR) proteins. Included among these are hydrolases, cell-wall strengthening proteins, proteins involved in oxidative burst, the combination of which are believed to promote heightened resistance. Biochemical and genetic analyses have identified genes and molecular signals associated with acquired resistance. The Npr1/Nim1 gene plays a key regulatory role in the AR defense in Arabidopsis against a broad spectrum of fungal and bacterial pathogens (WO 98/06748; WO 94/16077; WO 98/26082). The central importance of Npr1 in dicots was further substantiated by transgenic overexpression of the cloned gene, which led to heightened disease resistance in Arabidopsis against both fungal and bacterial pathogens (WO 98/06748).
Although the bulk of AR research has defined the pathway in dicotyledonous plants, monocotyledonous plants, such as wheat, rice, and barley, have an inducible pathway that protects against pathogen attack. Acquired resistance can be conditioned by different external stimuli, including avirulent pathogen challenge, pathogen elicitor exposure, and chemical treatments, including application of SA or SA analogs, such as 2,6-dichloroisonicotinic acid (INA) or benzo(1,2,3) thiodiazole-7-carbothioic acid S-methyl ester (BTH). Given the inducibility of the AR pathway by the same classes of activating compounds in monocot and dicot plants, there is likely to be partial conservation of signaling pathways, as subsets of PR genes appear to be induced in both groups. In monocots, induced acquired resistance is broad-spectrum, extending to fungal and bacterial pests, irrespective of pathogen race, with activated resistance persisting for weeks to months. Thus, manipulation of the AR pathway in plants may promote resistance to pathogens for which there exists no genetic source of resistance.
Thus, there is a need to identify genes that may play key roles in disease defense. Expression of these genes in transgenic plants may enhance the level of disease resistance against certain pathogens.
Within the past decade, the mechanisms by which plants activate innate immunity have been found to share a number of similarities with the innate immune responses of animals (Nimchuk et al., Annu. Rev. Gen. 37:579-609, 2003; Jones and Takemoto, Curr. Opin. Immun. 16:48-62, 2004; Nürnberger and Scheel, Trends Plant Sci. 8:372-379, 2001; Nürnberger et al., Immun. Rev. 198:249-266, 2004; Guttman, Biotech. Adv. 22:363-382, 2004; Staskawicz et al., Science 292:2285-2289, 2001; Nürnberger and Brunner, Curr. Opin. Plant Biol. 5:1-7, 2002). Innate immunity is initiated in animals and plants through the recognition of a variety of pathogen associated molecules that in animals are called “pathogen-associated molecular patterns,” or PAMPS, and in plants are called elicitors. Peptides derived from pathogens can be powerful elicitors of plant defense responses (Hahlbrock et al., Proc. Natl. Acad. Sci. USA 92:4150-4157, 1995; van den Askerveken et al. Plant Physiol. 103:91-96, 1993; Kammpren, Curr. Opin. Plant Biol. 4:295-300, 2001; Kunze et al., Plant Cell, 16:3496-3507, 2004; Navarro et al., Plant Physiol. 135:1113-1128, 2004; Fellbrich et al., Plant J. 32:375-390, 2002); He et al., Cell 73:1255-1266, 1993).
We previously identified a number of novel defense signal peptides from dicot and monocot plant species that are useful for enhancing plant resistance against various biotic or abiotic stresses, including, but not limited to, disease resistance. See U.S. provisional patent application Ser. No. 06/647,708, filed Jan. 26, 2005, and PCT/US2006/002661, filed Jan. 24, 2006.